In this regard, in an animal model of AMD (induced by 4-hydroxynonenal, 4-HNE), genetic deficiency of PTX3 led to enhanced complement activation, increased levels of C3a (a potent anaphylatoxin originating from proteolysis of C3) and the inflammatory cytokine IL-1β in the RPE, and accumulation of macrophages in the choroid (Wang et al., 2016), whereby PTX3 has been proposed to act as an anchoring molecule for FH in the BrM and RPE. The gene discussed is C3; the disease is age-related macular degeneration.